EKG of the month.
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Biomedical subjects
Publications and source records attributed to R M Gunnar.
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Various pharmacologic interventions that suppressed chemotactic factor activity in the coronary sinus after acute ischemia were analyzed for protective effects on myocardium. Ischemic injury was determined by comparing the slopes of the regression lines derived from 24 hour myocardial creatine kinase content versus S-T segment elevation 15 minutes after coronary ligation. Dogs treated 30 minutes after ligation with cobra venom factor, hydrocortisone or Trasylol showed a marked decrease in chemotactic activity in the coronary sinus. These agents also showed a protective effect on ischemic injury when compared to control. Myocardial biopsy specimens from areas of significant ischemia defined by S-T segment elevations in dogs treated with cobra venom factor were essentially devoid of an inflammatory response whereas those from dogs treated with Trasylol or hydrocortisone showed moderate neutrophil infiltration and minimal tissue exudate.
Thirty-seven patients in cardiogenic shock due to acute myocardial infarction were treated with intraaortic balloon counterpulsation and/or surgery. Eighteen of these patients were treated with counterpulsation alone; eight survived and five were in functional class I or II at the time of follow-up; two were in functional class III, and one was in functional class IV. Nineteen patients were treated surgically, eight survived and seven were in functional class I or II at the time of follow-up; one was in functional class III. Good functional recovery with counterpulsation alone is most common with inferior infarction. With surgery, functional recovery depends not only on the extent of the infarction and the coronary anatomy, but also on the ability to perform surgery within 12 hours of infarction or to support the patient with mechanical means for 10 to 14 days after the infarction and then perform surgery.
The effects of occlusion of the left anterior descending coronary artery on pulmonary hemodynamics and calculated pulmonary vascular resistance were measured in 17 open chest dogs anesthetized with chloralose. Coronary occlusion was associated with a slight but insignificant increase in mean pulmonary arterial pressure together with a significant elevation in mean left atrial pressure (P less than 0.01) and a significant reduction in mean pulmonary flow (P less than 0.01). Calculated pulmonary vascular resistance was significantly reduced during occlusion (P less than 0.01). The reduction in resistance was associated with elevated mean left atrial pressure and therefore reflected passive distension of pulmonary vessels secondary to suppressed left ventricular function. In contrast, coronary occlusion after vagotomy was not associated with a significant reduction in pulmonary vascular resistance, and in six experiments the decrease in resistance was converted to an increase. It is concluded that, before vagotomy, pulmonary hemodynamics during coronary occlusion are primarily affected through passive vessel distension whereas, after vagotomy tonic suppression of sympathetic activity is interrupted, thereby allowing enhancement of sympathetic vasoconstrictor activity to the pulmonary vascular bed and producing an increase in calculated resistance.
The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.
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To understand the hemodynamic changes produced by arrhythmias is to understand cardiovascular physiology. The changes in rate are accompanied by changes in contractility, receptor stimulation, peripheral vascular response, and flow to other vital organs. In addition, one must keep in mind the underlying pathology of the cardiovascular system. As a therapeutic program is initiated and adjusted, it must be done in accordance with the changes produced in the hemodynamics as well as the rhythm.